Drug Delivery Using Platelet Cancer Cell Interaction

Sarkar, Sounik; Alam, Aftab; Shaw, Jyoti; Dasgupta, Anjan Kr.

doi:10.1007/s11095-013-1097-1

Cited by 85 publications

(65 citation statements)

References 26 publications

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“…The ascetic fluid is the direct nutritional source for carcinoma development because it meets the nutritional requirements of carcinoma cells. In a cytological study, Ehrlich cells showed induced mitotic cells and cellular changes and a rapid increase ascetic fluid volume in EAC untreated group according to Funasaka et al, Osman et al, and Sarkar et al who reported that the aggregation of ascetic fluid in the peritoneal cavity was either due to a decreased lymphatic recovery system which is linked with the crippling of the lymphatic by carcinoma cells, or because angiogenesis which detected in ascites tumor‐bearing peritoneal wall, or either due to microvessels hyperpermeability of the peritoneal cavity.…”

Section: Discussionmentioning

confidence: 95%

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

Mutar

Tousson

Hafez

et al. 2019

Environmental Toxicology

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Cancer is the major cause of death and many factors that lead to its occurrences, such as environmental pollution and pesticides and other factors. Ehrlich carcinoma development depends on many things associated with the environment, nutrition, personal habits, and family history. The present study aimed to evaluate the potential protective effects of vitamin B17 (VB17) against Ehrlich ascites carcinoma (EAC) that induced kidney toxicity in female mice. The mice were divided into five groups (first group, control group; second group, VB17 group; third group, EAC group; fourth group, pretreated EAC with VB17; fifth group, cotreated EAC with VB17). Results showed the VB17 in pretreated (G4) and cotreated (G5) groups lead to an improvement in DNA damage and cytological examination, in addition significantly (P < .05) increase in Na+, red blood cell, hemoglobin, hematocrit value, mean corpuscular hemoglobin (MCH), and MCH concentration, whereas significantly (P < .05) decrease in urea, creatinine, K+, platelets, and white blood cells while insignificant (P < .05) changes in mean corpuscular volume when compared to the EAC group. Many histopathological changes were observed in kidney sections in EAC as marked damage and degenerated, glomerular atrophy, the Malpighian corpuscles that lost their characteristic configuration. On the other hand, a moderate improvement and arrangement in the kidney histological structure in pretreated VB17 + EAC, while a mild enhancement and arrangement of the kidney structure in cotreated EAC + VB17. In addition, depletion in renal P53 and PCNA protein expression compared with the EAC group. It could be concluded that VB17 has a potential renal protective effect against EAC cells induced kidney injury.

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Section: Discussionmentioning

confidence: 95%

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

Mutar

Tousson

Hafez

et al. 2019

Environmental Toxicology

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“…). This should, however, not prevent us making a good use of the close engagements of platelets with cancer cells, to develop platelet‐targeted anti‐cancer agents and to utilize platelets as a carrier of anti‐cancer agents, which have been proposed and investigated before . For example, utilizing the properties of cancer cell‐induced platelet activation and high co‐localization rate of platelets at the invasive front of cancer and/or with metastatic niches/foci of cancer cells, development of activated platelet‐targeting carrier of anti‐cancer drugs will be an attractive approach for the guided anti‐cancer therapies.…”

Section: Research Perspectivesmentioning

confidence: 99%

Platelets in cancer metastasis: To help the “villain” to do evil

2015

Int. J. Cancer

181

191

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Cancer progress is accompanied by platelet activation and thrombotic complications. Platelets are a dangerous alliance of cancer cells, and are a close engager in multiple processes of cancer metastasis. Platelet adhesion to cancer cells forms a protective cloak that helps cancer cells to escape immune surveillance and natural killer cell-mediated cytolysis. Platelets facilitate tethering and arrest of disseminated cancer cells in the vasculature, enhance invasive potentials and thus extravasation of cancer cells. Moreover, platelets recruit monocytes and granulocytes to the sites of cancer cell arrest, and collaborate with them to establish a pro-metastatic microenvironment and metastatic niches. Platelets also secret a number of growth factors to stimulate cancer cell proliferation, release various angiogenic regulators to regulate tumor angiogenesis and subsequently promote cancer growth and progress. Albeit platelets are helping the "villain" cancer to do evil, the close engagements of platelets in cancer metastasis and progress can be used as the intervention targets for new anti-cancer therapeutic developments. Platelet-targeted anti-cancer strategy may bring in novel anti-cancer treatments that can synergize the therapeutic effects of chemotherapies and surgical treatments of cancer.

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“…Despite the key role of PLTs in the maintenance of hemostasis, they were shown to regulate multiple processes such as angiogenesis, cell differentiation, cell migration, immune responses and tissue remodeling (25)(26)(27). More recently, those PLT unique features have been exploited in the development of novel therapies such as in supporting wound healing, tissue regeneration or as drug carriers (28)(29)(30)(31). Due to the population aging, a significant increase on PLT demand for all those therapeutic approaches is expected.…”

Section: Hla-universal Mks Generate Plts In a Refractoriness Mouse Modelmentioning

confidence: 99%

Generation of HLA-Universal iPSC-Derived Megakaryocytes and Platelets for Survival Under Refractoriness Conditions

Börger

Eicke

Wolf

et al. 2016

Mol Med

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Platelet (PLT) transfusion is indispensable to maintain homeostasis in thrombocytopenic patients. However, PLT transfusion refractoriness is a common life-threatening condition observed in multitransfused patients. The most frequent immune cause for PLT transfusion refractoriness is the presence of alloantibodies specific for human leukocyte antigen (HLA) class I epitopes. Here, we have silenced the expression of HLA class I to generate a stable HLA-universal induced pluripotent stem cell (iPSC) line that can be used as a renewable cell source for the generation of low immunogenic cell products. The expression of HLA class I was silenced by up to 82% and remained stable during iPSC cultivation. In this study, we have focused on the generation of megakaryocytes (MK) and PLTs from a HLA-universal iPSC source under feeder-and xeno-free conditions. On d 19, differentiation rates of MKs and PLTs with means of 58% and 76% were observed, respectively. HLA-universal iPSC-derived MKs showed polyploidy with DNA contents higher than 4n and formed proPLTs. Importantly, differentiated MKs remained silenced for HLA class I expression. HLA-universal MKs produced functional PLTs. Notably, iPSC-derived HLA-universal MKs were capable to escape antibody-mediated complement-and cellular-dependent cytotoxicity. Furthermore, HLA-universal MKs were able to produce PLTs after in vivo transfusion in a mouse model indicating that they might be used as an alternative to PLT transfusion. Thus, in vitro produced low immunogenic MKs and PLTs may become an alternative to PLT donation in PLT-based therapies and an important component in the management of severe alloimmunized patients.

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Drug Delivery Using Platelet Cancer Cell Interaction

Abstract: The proposed drug delivery strategy may lead to clinical improvement in the management of cancer treatment as lower drug concentration can be used in a targeted mode. Additionally the method can be personalized as patient's own platelet can be used for deliver various drugs.

Cited by 85 publications

References 26 publications

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

Ameliorative effects of vitamin B17 on the kidney against Ehrlich ascites carcinoma induced renal toxicity in mice

Platelets in cancer metastasis: To help the “villain” to do evil

Generation of HLA-Universal iPSC-Derived Megakaryocytes and Platelets for Survival Under Refractoriness Conditions

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